DSP(redirected from PPKS2)
Also found in: Dictionary, Encyclopedia.
DSPA gene on chromosome 6pter-p21 that encodes desmoplakin, an obligate component of functional desmosomes that anchors intermediate filaments to desmosomal plaques. Desmoplakin’s N-terminus is required for localisation to the desmosome and interacts with the N-terminal region of plakophilin 1 and plakoglobin. The C-terminus binds with intermediate filaments.
DSP mutations cause several cardiomyopathies, keratodermas and paraneoplastic pemphigus.
Poisoning should be suspected in many clinical circumstances but esp. when a patient has otherwise unexplained alterations in consciousness. The standard care of the poisoned patient begins with immediate stabilization of the patient's airway, breathing, circulation, and neurological status if these are compromised. This may require oximetry, blood gas analysis, electrocardiographic monitoring, airway placement, endotracheal intubation, fluid resuscitation, administration of naloxone and dextrose, or the use of pressors for some severely intoxicated patients. If the poison can be identified, reference texts or local poison control centers should be contacted to determine specific antidotes or treatments. When the poison is unidentified or when rescuers are uncertain about its cause, it is safest to test blood and urine for acetaminophen, aspirin, and commonly abused drugs. Blood testing should also include assessments of electrolytes, kidney function, liver function, and a complete blood count. Women of childbearing age should also be routinely screened for pregnancy.
Decontamination of the gastrointestinal tract includes activated charcoal if the patient has ingested a drug or chemical to which the charcoal can bind; or whole bowel irrigation, which sweeps toxins from the bowel before they are absorbed. Inducing vomiting, formerly relied on in poisonings, is now rarely used because it has not been shown to improve outcome and may cause complications such as aspiration pneumonia. After decontamination procedures, specific antidotes, if available, should be administered.
The elimination of many drugs from the body can be enhanced by other means, including the administration of alkaline fluids, hemodialysis, or hemoperfusion.
Once the patient is stabilized, the cause for the intoxication should be addressed. Patients with substance abuse problems should be referred for detoxification, support, and counseling; suicidal and depressed patients may benefit from counseling or drug therapy. Demented patients who have poisoned themselves because of confusion about their medications should have the administration of their medications supervised. In some cases, poisonings are iatrogenic
CAUTION!Many illnesses (such as massive strokes, postictal states, insulin reactions, sepsis, meningitis, uremia) mimic the symptoms of poisoning, esp. when the patient has altered mental status.
Shortly after ingestion, patients may suffer nausea, vomiting, and malaise. If appropriate treatment is not instituted, hepatitis develops, with elevated liver enzymes in the first day, and jaundice and coagulation disorders by about 36 hr. Encephalopathy may follow. A prolonged course of recovery or complete liver failure may result, depending on the amount of drug ingested and the severity of the liver injury.
Gastrointestinal (GI) decontamination with activated charcoal absorbs toxin from the GI tract, but it should be given within 4 hr of ingestion of the drug. A specific antidote, N-acetylcysteine, is given orally within 8 to 10 hr after ingestion in an initial dose of 140 mg/kg and then in 70 mg/kg doses every 4 hr for 17 doses if acetaminophen levels are toxic. Alternatively, acetylcysteine may be administered intravenously. Blood should be drawn for stat acetaminophen level, complete blood count, electrolyte levels, blood urea nitrogen, serum creatinine, serum glucose, liver function, prothrombin time, and further toxicology screens. Urine should also be analyzed for drug content. If the patient with a suspected overdose is a female of child-bearing age, a pregnancy test should be done as a part of routine laboratory studies. The overdosed patient should be cared for in an intensive care unit until medically and psychiatrically cleared for discharge. ; Rumack nomogram
CAUTION!Taking more than 4 g of acetaminophen in one day (adults) or more than 90 mg/kg (children) can damage the liver and may lead to coma, kidney failure, and death.
Irrigate exposed skin with soap and water, e.g., in the safety shower. Support breathing and oxygenation. Notify the local poison control center.
acetylsalicylic acid poisoningAspirin poisoning.
Dilute with large volumes of water. Give demulcents and morphine for pain. Treat as a chemical burn.
CAUTION!The use of emetics and stomach tubes is contraindicated.
acute cocaine hydrochloride poisoning
An overdose of cocaine is an accelerated version of the classic physiological and psychological responses to cocaine use. Initial euphoria is followed by excitability, delirium, tremors, convulsions, tachycardia, and angina pectoris, all of which are signs of overwhelming sympathetic stimulation of the brain, heart, and lungs. Death is usually caused by a cardiovascular event or to respiratory failure. Plasma and liver pseudocholinesterase detoxify cocaine into water-soluble metabolites that are excreted in urine. Anyone with low plasma cholinesterase activity (such as a fetus, infant, pregnant woman, or someone with liver disease) is very prone to cocaine toxicity. People who congenitally lack pseudocholinesterase are highly sensitive to the effects of any dose of cocaine.
Many chronic cocaine users overdose while taking no more than their usual amount of the drug, when, e.g., the purity (pharmacological strength) of an ingested dose is greater than usual or the drug has been mixed with another psychoactive substance. Lethal overdoses are usually caused by acute coronary syndromes. Some cocaine users may die instead of intracerebral hemorrhage. The presenting findings may include seizures, hemiplegia, aphasia, or coma. Patients admitted for trauma may also be cocaine intoxicated (two thirds of cocaine-related deaths result from traumatic injuries, not drug overdose). Because many signs and symptoms that cocaine produces resemble those from injuries, and because cocaine poisoning is life-threatening, emergency department care providers must quickly distinguish drug-related problems from traumatic injury problems.
Oxygen and aspirin should be given with benzodiazepines to reduce agitation and calcium channel blockers to reduce high blood pressure. Beta blockers should be avoided.
Vital signs are checked frequently, the patient is attached to a cardiac monitor, and an intravenous line is initiated. Large volumes of fluids are infused to help remove protein breakdown products from the body (a result of rhabdomyolysis). Bilateral lung sounds are auscultated frequently during fluid resuscitation because aggressive fluid therapy can worsen heart failure. Care providers try to physically control patients to prevent them from injuring themselves. If patients demonstrate violent or aggressive behavior, chemical or physical restraints may be necessary. Calcium channel blockers or a benzodiazepine is administered as prescribed to reduce the patient's blood pressure and heart rate. Seizures, which occur because the seizure threshold is lowered by cocaine, are treated with diazepam. Because cocaine causes hypothalamic thermal regulatory dysfunction, core body temperature must be monitored closely. Elevated temperature is treated with acetaminophen and cooling blankets, cool-air ventilation, and cool saline gastric lavage. Central Nervous System (CNS) stimulation may be followed by CNS depression (flaccid paralysis, coma, fixed and dilated pupils, respiratory failure, and cardiovascular collapse).
Cocaine smuggling often involves body packing (swallowing balloons, condoms, or other objects filled with cocaine). If these items leak, the patient becomes intoxicated and is at high risk for death.
If the patient survives the acute poisoning episode, treatment is directed toward helping the patient abstain from drugs and preventing relapses. The patient benefits from consultation with an addictions specialist or mental health nurse practitioner. Studies support the effectiveness of a 12-step program, such as Cocaine Anonymous, to help build a solid recovery program. Other community resources also can be accessed to provide various types of support and to help the patient identify and manage relapse triggers.
acute lead poisoning
Adequate urine flow should be established; convulsions may be controlled with diazepam. Calcium disodium edetate and dimercaprol are administered to remove lead from the body. After acute therapy is completed, penicillamine is given orally for 3 to 6 months for children and up to 2 months for adults. The exposure to lead should be reduced or eliminated.
CAUTION!Patients receiving penicillamine therapy must be monitored weekly for adverse reactions, including diffuse erythematous rashes, angioneurotic edema, proteinuria, and neutropenia. Penicillamine is contraindicated in patients with a history of penicillin sensitivity, renal disease, or both.
acute nicotine poisoning
Nausea, salivation, abdominal pain, vomiting, diarrhea, sweating, dizziness, and mental confusion. If the dose is sufficient, the patient will collapse, develop shock, convulse, and die of respiratory failure caused by paralysis of respiratory muscles.
Activated charcoal may be given to conscious patients who are not vomiting. Unconscious patients should be intubated and supported in an intensive care unit. Anticonvulsants are used to treat seizures.
Large amounts of water are given by mouth. Consultation with an ear, nose, and throat specialist is often advisable. Tracheostomy or intubation is performed if necessary to protect the airway. Morphine is useful to allay pain. Rest, heat, quiet, and adequate fluid intake are necessary.
CAUTION!Emetics, strong acids, and lavage should be avoided. Fluid balance and electrolytes should be carefully monitored.
amnesic shellfish poisoning
British antilewisite can be used as an antidote.
Symptoms include a burning pain throughout the gastrointestinal tract, vomiting, dehydration, shock, dysrhythmias, coma, convulsions, paralysis, and death.
The stomach should be lavaged with copious amounts of water. Dimercaprol (British antilewisite) or other chelators (such as penicillamine) should be given immediately.
After first aid, fluid and electrolyte balance must be maintained. Morphine should be given for pain. The patient is treated for shock and pulmonary edema. Blood transfusion may be required. arsenic in
arum family poisoning
Activated charcoal is given by mouth. Intravenous (IV) fluids are given for dehydration but must not be overloaded. Enough IV fluids should be given to establish 3 to 4 ml/kg/hr of urine flow. Alkalinization of urine is achieved by administering bicarbonate. The goal is a urine pH of 8 or higher. After urine flow is established, potassium 30 mEq/L of administered fluid should be added. After serum potassium levels reach 5 mEq/L, potassium should be discontinued. If alkalinization of the urine is not attained, hemodialysis may be needed. Synonym: acetylsalicylic acid poisoning
atropine sulfate poisoning
Oxygen is given; a cardiac monitor, oximeter, and automated blood pressure cuff are applied; and intravenous fluids are administered. Patients experiencing restlessness may respond to the administration of a benzodiazepine (such as lorazepam or diazepam). If the atropine has been ingested orally, gastric lavage with activated charcoal may absorb some of the toxin from the gastrointestinal tract. Severe neurological side effects (such as seizures) may be treated with physostigmine.
When oxygenation and ventilation are compromised, intubation and mechanical ventilation may be needed. Other supportive treatments include activated charcoal, bicarbonate-containing fluids (to make the urine alkaline and increase barbiturate excretion), rewarming techniques, and fluids or drugs to support blood pressure.
Symptoms include metallic taste, foul breath, fever, gastrointestinal irritation, a bluish line at the gum margin, ulcerative process of the gums and mouth, headache, and renal tubular damage.
The source of bismuth is removed; gastric lavage and/or activated charcoal are given; respiratory support and chelation therapy with British antilewisite (BAL) are provided.
boric acid poisoning
Symptoms include nausea, vomiting, diarrhea, convulsions, weakness, central nervous system depression, livid skin rash characterized as “boiled lobster rash, ” and shock. Acute renal failure and cardiac failure may result from large ingestions.
Activated charcoal may prevent absorption of boric acid from the gastrointestinal tract. Hemodialysis is sometimes required for severe intoxications.
CAUTION!Call the nearest poison control center to determine proper therapy.
Hemorrhage is the most common side effect and may occasionally be life-threatening. Bleeding within the kidneys and urinary tract produces acute renal failure.
Because warfarin interferes with the liver's use of vitamin K to produce clotting factors, brodifacoum poisoning is treated with vitamin K, fresh frozen plasma, and supportive therapy.
Symptoms include vomiting, abdominal pain, respiratory and eye irritation if inhaled, corrosion of the mouth and intestinal tract if swallowed, cyanosis, tachycardia, and shock.
If bromide is inhaled, oxygen is administered, respiratory support provided, and pulmonary edema treated. If bromide is swallowed, gastric lavage may reduce intestinal absorption.
carbon dioxide poisoning
Symptoms include a sensation of pressure in the head, ringing in the ears, an acid taste in the mouth, and a slight burning in the nose. With massive exposures to very concentrated CO2, respiratory depression and coma may occur.
The patient should be removed to fresh air and given oxygen and, if needed, ventilatory assistance.
carbon monoxide poisoning
CAUTION!Pulse oximetry is not a useful measure in CO intoxication: it cannot differentiate between carboxyhemoglobin and oxyhemoglobin and therefore gives a falsely elevated indication of oxygenation.
The symptoms of CO poisoning vary with the level of exposure and the concentration of COHb in the bloodstream. At levels of less than 10%, patients may be symptom-free or may complain only of headache. (Heavy cigarette smoking may produce levels as high as 7% to 9%.) COHb levels of 30% produce mild neurological impairment (dizziness, fatigue, difficulty concentrating), and levels of 50% may cause seizures or coma. Death is likely when COHb levels exceed 70%.
Arterial or venous COHb levels should be obtained immediately, and serial levels checked hourly to monitor treatment effectiveness. Blood glucose, ethyl alcohol, acetaminophen, and other drug levels should be measured on all patients who come to the ER with altered mental status. Computed tomography or MR imaging of the brain may also be necessary. The patient should be removed immediately from exposure to CO. If the patient has severe CO poisoning (indicated by carboxyhemoglobin levels above 25%) or cardiovascular and neurologic impairment regardless of levels, hyperbaric oxygen therapy should be employed if available, and the patient admitted to the hospital. 100% oxygen is given with a tight-fitting non-rebreather mask, under pressure (hyperbaric) if possible. Intubation and mechanical ventilation should be used if indicated. A venous access is used to provide saline infusion, and cardiac and hemodynamic monitoring is established. The patient should be kept at bedrest to reduce the body's oxygen requirements.
Potential complications of hyperbaric therapy include sinus and middle ear barotrauma, hyperoxic seizure, anxiety, and oxidative stress. Intubation and mechanical ventilation should be used for patients with diminished level of consciousness or respiratory distress, esp. if hyperbaric treatment is not available. An antiemetic may be prescribed to manage nausea and prevent vomiting. Bedrest limits exertion and tissue oxygen demand, reducing organ ischemia. Patients with cardiac or renal disease are necessarily at increased risk for CO complications. In general, people with more severe initial symptoms are at higher risk for sequelae.
Clinical improvement after treatment is indicated by the presence of hemodynamic stability without IV support, mechanical ventilation, or supplemental oxygen; sufficient urine output; the return of an appetite; and a stable neurological status. A follow-up visit with a health care professional is advisable shortly after discharge. Patients should be taught about the major causes of CO exposure and should not return home until the source of carbon monoxide has been eliminated, e.g., by a certified heating and ventilation specialist. The importance of having the home heating furnace inspected and cleaned annually should be stressed. Patients should also be cautioned about working on an automobile in a garage with the engine running or burning items indoors. The Consumer Product Safety Commission recommends that CO detectors be installed on each level of the home and just outside the sleeping areas. Most are battery operated and easily installed. Patients should be advised to evacuate the home if an alarm sounds, leaving windows or doors open for ventilation, and to call 911. Alarms should never be turned off or ignored, and batteries should be replaced when the clocks are changed in spring and fall, as for smoke alarms. See: table
|Carbon Monoxide Concentration in Air|
|Percent in Air||Parts per Million||Comment|
|0.005||50||Occupational Safety and Health Administration (OSHA) maximum permissible exposure limit averaged over an 8-hr day|
|0.01||100||OSHA standard: Maritime worker peak concentration limit|
|0.02||200||OSHA standard: Brief exposures during loading and unloading cargo are permissible|
|0.04||400||The level of CO in cigarette smoke is eight times higher than the OSHA permissible exposure limit|
|0.08||800||Headache, dizziness, and nausea in 45 min; collapse and possible unconsciousness in 2 hr|
|0.16||1600||Headache, dizziness, and nausea in 20 min; collapse and possible death in 2 hr|
|0.32||3200||Headache and dizziness in 5–10 min; unconsciousness and possible death in 10–15 min|
|0.64||6400||Headache and dizziness in 1–2 min; possible death in 10–15 min|
|1.28||12,800||Immediate unconsciousness; possible death in 1–3 min|
carbon tetrachloride poisoning
Clothes contaminated with carbon tetrachloride are removed. Oxygen, artificial respiration, gastric decontamination, and management of cardiac rhythms are often needed.
chloral hydrate poisoning
An airway must be maintained and a cuffed endotracheal tube used if necessary. Mechanical ventilation may be required. A slurry of activated charcoal is administered. Beta blockers (e.g., propranolol) are used to manage arrhythmias.
chronic lead poisoning
Exposure to lead should be eliminated and an adequate diet with added vitamins provided. Chelating agents such as dimercaprol, dimercaptosuccinic acid (succimer), or EDTA are given to reduce lead levels to normal.
A history is obtained to determine whether the sources of lead ingestion or inhalation are caused by the environment, work, or folk remedies, and preparations are made for their removal. (In many states, removal of household lead must be done by state-licensed specialists, not homeowners. The CDC and local poison-control centers provide relevant information. A 1-cm square chip of lead-based paint may contain a thousand times the usual safe daily ingestion of lead.) A history is obtained of pica; recent behavioral changes, particularly, in children, a lack of interest in playing; and behavioral problems such as aggression and hyperirritability. The patient is assessed for developmental delays or loss of acquired skills, esp. speech. central nervous system signs indicative of lead toxicity may be irreversible. The younger child is assessed for at-risk characteristics such as the high level of oral activity in late infancy and toddlerhood; small stature, which enhances inhalation of contaminated dust and dirt in areas heavily contaminated with lead; and nutritional deficiencies of calcium, zinc, and iron, the single most important predisposing factor for increased lead absorption. Older children are assessed for gasoline sniffing, which is esp. prevalent among children in some cultures. The parent-child interaction is assessed for indications of inadequate child care, including poor hygienic practices, insufficient feeding to promote adequate nutrition, infrequent use of medical facilities, insufficient rest, less use of resources for child stimulation, less affection, and immature attitudes toward maintaining discipline. Prescribed chelating agents are administered to mobilize lead from the blood and soft tissues by enhancing its deposition in bones and its excretion in urine. A combination of drugs may result in fewer side effects and better removal of lead from the brain. If encephalopathy is present, fluid volume is restricted to prevent additional cerebral edema. Injections are administered intramuscularly, and injection sites are rotated for painful injections (which may include simultaneous procaine injection for local anesthesia). The child is allowed to express pain and anger, and physical and emotional comfort measures are provided to relieve related distress. If there is no encephalopathy, injections are administered intravenously, and hydration is maintained. The patient is evaluated for desired drug effects measured by blood levels and urinary excretion of lead and for signs of toxicity from the chelating agents. (Special blood collection and urine collection containers are necessary for some of the monitoring tests. The laboratory should be consulted before collection.) . Prescribed anticonvulsants are administered as necessary to control seizures (often severe and protracted), an antiemetic for nausea and vomiting, an antispasmodic for muscle cramps, and analgesics and muscle relaxants for muscle and joint pain. Serum electrolytes are monitored daily, and renal function is evaluated frequently. Whole bowel irrigation is used when lead is visible in the GI tract (or for episodes of acute lead ingestion). Adequate nutrition is provided, and nutritional deficiencies are corrected, by administering prescribed supplements (e.g., of iron). An active, active-assisted, or passive range-of-motion exercise program is established to maintain joint mobility and prevent muscle atrophy. Parents are taught and supported to prevent recurrence, and the public is educated about the dangers of lead ingestion, the importance of screening young (esp. preschool) children at risk, the signs and symptoms indicative of toxicity, and the need for treatment.
codeine poisoningopiate poisoning;
cone shell poisoning
copper sulfate poisoning
Penicillamine or dimercaprol should be given. The caregiver should monitor vital signs, treat shock, administer oxygen if needed, control convulsions, and maintain electrolyte balance.
This type of poisoning is marked by intense burning of the mouth, throat, pharynx, and abdomen; abdominal cramping, retching, nausea, and vomiting, and often collapse. There may be hematemesis and diarrhea; the stools are watery, mucoid, bloody, and possibly stained with the poison or its products, resulting from its action on the contents of the alimentary tract. Stains of the lips, cheeks, tongue, mouth, or pharynx are often a characteristic brown; stains on the mucous membranes may be violet or black. Carbolic acid (phenol) stains are white or gray, resembling boiled meat; hydrochloric acid stains are grayish, nitric acid, yellow; sulfuric acid leaves tan or dark burns.
Immediate treatment in a hospital is mandatory. It is important to try to discover the chemical substance ingested, and all materials such as food, bottles, jars, or containers should be saved. This is essential if the patient is comatose or an infant.
CAUTION!In treating corrosive poisoning, vomiting must not be induced; gastric lavage must not be attempted; and no attempt should be made to neutralize the corrosive substance.
Vomiting will increase the severity of damage to the esophagus by renewing contact with the corrosive substance. Gastric lavage may cause the esophagus or stomach to perforate. If the trachea has been damaged, tracheostomy may be needed. Emergency surgery must be considered if there are signs of possible perforation of the esophagus or of the abdominal viscera. Opiates will be needed to control pain. For esophageal burns, broad-spectrum antibiotic and corticosteroid therapy should be started. Intravenous fluids will be required if esophageal or gastric damage prevents ingestion of liquids. Long-range therapy will be directed toward preventing or treating esophageal scars and strictures.
The most common patients are jewelers, metal platers, those who handle rodenticides, victims of smoke inhalation, and patients treated with very high doses of sodium nitroprusside. Rarely, cyanide poisoning results from the ingestion of certain fruits (e.g., the bitter cassava and some stone fruits).
Palpitations, disorientation, and confusion may be rapidly followed by respiratory failure, seizures, coma, and death in patients who suffer large exposures. Smaller exposures may produce anxiety, dizziness, headache, and shortness of breath. Patients may report that they have detected an odor of bitter almonds at the time of exposure to cyanide.
The patient is immediately treated with gastric lavage, and activated charcoal is given to adsorb to whatever toxin may remain in the gastrointestinal tract. Emesis is contraindicated. Oxygen is immediately provided; intubation and mechanical ventilation may be needed when the patient has suffered respiratory failure. Antidotes to cyanide poisoning include hydroxocobalmin and sodium thiosulfate.
diarrheal shellfish poisoningAbbreviation: DSP
Extracardiac signs develop initially in most patients, the first of which is almost always anorexia. Nausea and vomiting, sometimes with abdominal pain and increased salivation, usually appear 1 to 2 days later. Other symptoms include fatigue, drowsiness, general muscle weakness, and visual disturbances such as blurring of vision, yellow-green or white halos around visual images, light flashes, photophobia, and diplopia. Mental disturbances (such as agitation, hallucinations, and disorientation) are very common in elderly atherosclerotic patients. If the early signs are unheeded, 80% of patients eventually will show more serious cardiac signs. Toxic concentrations of digitalis can cause nearly every known arrhythmia. They can decrease heart rate by slowing conduction and increasing the refractory period at the AV node, or they can increase the rate by creating abnormal pacemaker activity in the conductive tissue.
The distinction between therapeutic and toxic levels digoxin is narrow; therefore, health care providers must be alert to signs of digitalis poisoning in patients. Elderly patients and those with liver or kidney disease are at esp. high risk because their absorption, metabolism, and excretion rates are unpredictable. Health care providers should consider health status changes that can alter a patient's response to digitalis, including vomiting, diarrhea, or other gastrointestinal upset; acid-base or electrolyte disturbances (such as hypokalemia, hypomagnesemia, or hypercalcemia), which alter the heart's sensitivity to digitalis; hypothyroidism, which disrupts the patient's ability to metabolize digitalis; and liver or kidney disease, which modifies metabolism and excretion. Changes in a treatment regimen also can predispose the patient to toxicity, esp. the addition of or increase in dosages of drugs such as antiarrhythmics, calcium channel blockers, or potassium-wasting diuretics. Assessment for digitalis toxicity is necessary if electrical cardioversion is used to restore a patient to sinus rhythm because this procedure increases the heart's sensitivity to digitalis.
Because digitalis toxicity develops quickly and insidiously, the patient is taught early symptoms to report. Extracardiac signs can be missed or mistaken for complications of another condition being treated, e.g., pneumonia. Health care providers need to compare the patient's current appetite and activity to the patient's previous health status, and carefully monitor the patient for electrolyte imbalances. Significant decreases or increases in heart rate and rhythmic irregularities must be reported because toxic concentrations may lead to ventricular fibrillation and death. If toxicity is suspected, an electrocardiogram is performed. Electrocardiographic signs of digitalis toxicity include first-degree atrioventricular (A-V) block with depressed S-T segments, shortened Q-T intervals, and flattened T waves. In the presence of such changes a serum digoxin level and basic chemistries may be used to confirm toxicity. Because hypokalemia is a major cause of digitalis toxicity, adequate potassium intake in the diet and prescribed supplementations are essential. The patient is advised about conditions such as diarrhea, which may deplete the body of potassium or contribute to dehydration and renal insufficiency. The patient is advised not to take over-the-counter medications without notifying his health care provider because these may alter his sensitivity to digitalis.
Digitalis poisoning may sometimes occur because of accidental or deliberate overdose. Emergency department personnel may sometimes remove the drug from the stomach by lavage or activated charcoal, administer intravenous fluids, provide potassium, monitor cardiac status, and/or treat cardiac arrhythmias as they arise. They may also administer digoxin immune FAB (ovine) to bind serum digoxin, preventing it from binding to cardiac receptors.
Within several hours of ingestion, the patient may develop anticholinergic symptoms (such as abdominal cramping, bradycardia, pupillary dilation, urinary retention) and vasoconstriction (with ischemia and gangrene of the extremities).
Sodium nitroprusside may counteract the vascular spasm produced by ergots.
Symptoms include local irritation of the eyes, nose, mouth, throat; respiratory and gastrointestinal tracts; central nervous system disorders (including vertigo, stupor, convulsions, unconsciousness); and renal damage.
The most hazardous symptom of gasoline exposure is a potentially fatal inflammation of the lungs, caused by aspiration of even small quantities of distilled petroleum. Symptoms of oral ingestion may also include dizziness, disorientation, seizures, and other neurological difficulties; gastric irritation and vomiting; rashes; and cardiac rhythm disturbances.
The patient should be observed for at least 6 hours. If no evidence of respiratory distress or dysfunction is found, and if a chest x-ray exam shows no signs of chemical pneumonitis, the patient may be safely discharged home.
Patients with evidence of chemical pneumonitis should be treated with oxygen and monitored in a hospital. Patients in full respiratory failure will require mechanical ventilation. Those who have deliberately ingested gasoline may benefit from supportive psychotherapy or psychiatric referral.
heavy metal poisoning
Oral activated charcoal may be given to decrease the absorption of the toxin from the gastrointestinal tract. Respiratory failure should be treated with intubation and mechanical ventilation. The local Poison Control Center should be contacted for additional instructions.
hypochlorite salt poisoning
The area should be washed with alcohol, soap, and water. It then should be rinsed carefully and covered with a bland dressing such as cold cream.
The patient should immediately be given by mouth a cornstarch or flour solution, 15 g in 500 ml (2 cups) of water. Activated charcoal or gastric lavage may also be employed.
The victim vomits, usually within an hour of taking the iron. Vomiting of blood and melena may occur. If untreated, restlessness, hypotension, rapid respirations, and cyanosis may develop, followed within a few hours by coma and death.
Whole bowel irrigation should be used to force ingested iron out of the gastrointestinal tract. Chelation of iron can be performed with deferoxamine, which binds circulating iron from the bloodstream.
ivy poisoningSee: poison ivy dermatitis
Acute poisoning: Seizures are treated with benzodiazepines. Fluid and electrolyte balance is maintained. Cerebral edema is treated with mannitol and dexamethasone. The blood lead level is determined. If it is above 50 to 60 µg/dl, the lead is removed from the body with a chelator, e.g., edetate calcium disodium, dimercaprol, D-penicillamine, or succimer [DMSA]. Succimer has the advantage of being orally active and is esp. helpful in treating children. The effect of treatment is monitored closely and may have to be continued for a week or longer or repeated if the lead level rebounds.Chronic lead poisoning: A blood lead level equal to or > 10 mcg/dL in a child may impair normal development of the central nervous system. Parents of exposed children should be educated about potential environmental or nutritional sources of lead exposure, and the child should be rechecked in a month. Rising levels, e.g., above 25 mcg/dL or higher, may warrant treatment with chelators. Public health officials should be notified when a child's lead level is elevated so that environmental remediation or relocation of the patient and family, as indicated, may be undertaken.
Symptoms include muscular weakness, difficulty walking, tremors, central nervous system disturbances, and salivation.
The child should be treated supportively, e.g., with oral fluids as tolerated and antiemetics if they are needed. See: phosphorus poisoning
mercuric chloride poisoning
Symptoms include severe gastrointestinal irritation with pain, cramping, constriction of the throat, vomiting, and a metallic taste in the mouth. Abdominal pain may be severe. Bloody diarrhea, bloody vomitus, scanty or absent urine output, prostration, convulsions, and unconsciousness may follow. Death from uremia is the usual outcome unless treatment is begun immediately.
Oxygen and intravenous fluids are given. Gastric lavage (not emesis) is used to empty the gastrointestinal tract. Dimercaprol or d-penicillamine is used for chelation. Similar treatment is given for mercurous chloride poisoning.
mercurous chloride poisoning
Gastric lavage or whole bowel irrigation may be used to empty the gastrointestinal tract. Hemodialysis or chelation therapy, e.g., with succimer or penicillamine, may also be helpful. mercuric chloride in
methyl alcohol poisoning
Fluids and electrolyte and acid-base balance should be carefully monitored and adjusted. Methanol may be removed from the bloodstream by hemodialysis.
mushroom poisoning,, mushroom and toadstool poisoning
The patient may experience brief exhilaration followed by drowsiness, respiratory depression, or coma, or, in massive overdoses, death.
An airway should be established and ventilation provided. A narcotic antagonist such as naloxone should be given.
nitric acid poisoning
Emergency measures include oral administration of activated charcoal and large volumes of water. Emetics and stomach tubes should be avoided because they may cause rupture of the esophagus or stomach.
The patient may experience brief mental exhilaration followed by drowsiness, respiratory depression, pulmonary edema, coma, or, in massive overdoses, death.
An airway should be established and ventilation provided. A narcotic antagonist such as naloxone is given, which may be repeated periodically if symptoms return. Pulmonary edema may be treated with diuretics, nitrates, and/or positive pressure ventilation. Synonym: codeine posioning; opium poisoning
opium poisoningOpiate poisoning.
oxalic acid poisoning
Signs and symptoms include a corrosive action on the mucosa of the mouth, esophagus, and stomach; a sour taste; burning in the mouth, throat, and stomach; great thirst; bloody vomitus; collapse; and, sometimes, convulsions and coma.
Gastric lavage should be used to empty the gastrointestinal tract. Activated charcoal can be given to bind the acid. Vomiting should not be induced.
There is no specific antidote. Supportive care includes airway management, ventilation, and hemodialysis.
paralytic shellfish poisoningAbbreviation: PSP
paregoric poisoningSee: opiate poisoning
The patient may present with coagulative necrosis of affected skin or mucous membranes or with evidence of internal organ damage.
Contaminated clothing should be removed immediately. The skin should then be irrigated with copious amounts of water and either isopropyl alcohol or a solution containing polyethylene glycol. Patients who have ingested phenols should be treated with activated charcoal to absorb as much toxin as possible and be given general supportive care. Consultation with specialists in toxicology, otorhinolaryngology, and critical care medicine, may be necessary in cases of massive or severe exposure.
Liver failure may follow acute irritation of the gastrointestinal tract. There may also be kidney damage. Other symptoms include profound weakness, hemorrhage, and heart failure. Occasionally nervous system symptoms predominate.
Gastric lavage is performed if phosphorus was swallowed. The airway is protected by cuffed endotracheal intubation. Charcoal and a cathartic drug are administered. Depending on the length of time since ingestion, intravenous fluids may be used to flush the poison out of the system by diuresis. In some cases, peritoneal or hemodialysis may be needed. The patient requires close monitoring for delayed effects for at least 24 hr. If the poison was intentionally ingested, the patient is placed on suicide precautions and referred for further psychological counseling.
potassium chlorate poisoning
CAUTION!Vomiting should not be induced.
potassium chromate poisoning
When taken by mouth, potassium chromate has a disagreeable taste; it causes cramping, pain, vomiting, diarrhea, slow respiration; and it may affect the liver and kidneys.
CAUTION!Vomiting should not be induced.
For ingestion, the patient is treated as if poisoned with a strong acid. Gastric lavage is administered through a nasogastric tube. Bronchoalveolar lavage or penicillamine may be used.
potassium hydroxide poisoning
CAUTION!Vomiting should not be induced.
The patient requires hospitalization, morphine for pain, and, often, treatment for shock. If the patient's airway has been burned, topical care is provided; tracheostomy may be required. Corticosterioids and antibiotics may be given.
red kidney bean poisoning
Patients who have overdosed on aspirin are treated with bicarbonate to increase the systemic pH and enhance excretion of salicylates in the urine. Hemodialysis is used to remove salicylates from the blood in life-threatening intoxications.
scombroid fish poisoning
Nausea, vomiting, abdominal cramps, diarrhea, flushing, headache, urticaria, a burning sensation and metallic taste in the mouth, dizziness, periorbital edema, and thirst may develop 30 min after eating the fish and last a few hours.
Antihistamines reverse many of the symptoms of the syndrome.
silver nitrate poisoning
sodium fluoride poisoning
The affected areas of the skin should be washed and the compound precipitated by addition to the wash solution of soluble calcium salts such as lime water, calcium gluconate, or calcium lactate.
staphylococcal food poisoning
Patients who contract food poisoning should ingest clear fluids until abdominal pain subsides and then gradually return to a normal diet. Fluid and electrolyte balance is monitored, and supportive therapy is maintained as indicated. Enteric precautions are used until evidence of infection subsides.
After the gastrointestinal tract is decontaminated with activated charcoal, stimulation of the intoxicated person should be minimized. Severely poisoned people (those with seizures, extremely high body temperatures, or cardiac dysrhythmias) may be treated with intravenous physostigmine, given slowly.
Overdoses should be treated with gastric decontamination, e.g., activated charcoal, and drugs, e.g., diazepam that limit muscular contraction. Supportive care includes intravenous hydration with alkalinization of the urine to prevent or treat the consequences of rhabdomyolysis.
sulfuric acid poisoning
Early local effects of acid injury, e.g., necrosis of the skin or the upper gastrointestinal tract, result from direct contact of sulfuric acid with the epithelium. The patient may complain of intense pain, e.g., in the mouth or throat. If acid contacts the eye, it may cause pain and corneal injury, sometimes resulting in blindness. Several days to 2 weeks after massive acid ingestion, perforation of internal organs may occur. When the stomach is involved, the perforation may leak acid into the mediastinum or peritoneum, causing pain, dyspnea, hypotension, tachycardia, or shock.
Exposed surfaces should be promptly washed in water to dilute the concentration of acid and minimize the depth of acid penetration. If the airway is compromised, the patient should be immediately intubated and ventilated, before undergoing dilutional therapy. Activated charcoal, which is helpful in many other exposures, is not useful. Neutralizing substances such as diluted alkalies are probably not helpful.
Most patients who ingest significant quantities of acid will undergo upper gastrointestinal endoscopy to evaluate the extent of the acid burn. Strictures, e.g., esophageal strictures, that develop as a result of scarring from acid burns are treated with dilation. People with ocular exposures need immediate ophthalmological consultation. Immediate surgery is warranted for patients with internal organ perforation.acids in
CAUTION!Blind nasogastric intubation is generally contraindicated because it may damage the upper gastrointestinal tract. Gastric intubation and lavage should be performed by experienced endoscopists.
Theophylline toxicity may occur if the patient's symptoms and drug levels while using compounds containing theophylline are not monitored regularly. Many commonly used drugs such as cimetidine, ciprofloxacin, erythromycin, and rifampin alter the metabolism of theophylline and may produce toxic reactions if they are taken during theophylline therapy; these drugs should be avoided. Because of the risk of theophylline poisoning, most patients with reactive airway diseases such as asthma or asthmatic bronchitis are treated with inhaled bronchodilators instead of theophylline.
The patient may require monitoring in a critical care unit, where blood pressure and cardiac rhythm can be observed closely and early interventions taken in the case of seizures or potentially fatal arrhythmias. Anticonvulsants are given for seizures (or to prevent seizures when theophylline levels exceed 100 mg/dl); the gastrointestinal tract should be decontaminated with activated charcoal, and antiarrhythmic drugs are administered, as indicated, for disturbances in cardiac rhythm. Severe overdoses or ones with refractory symptoms should be treated with charcoal hemoperfusion.
tincture of iodine poisoningIodine poisoning.
toadstool poisoningMushroom poisoning.
Symptoms include a warm or burning sensation in the esophagus and stomach, followed by cramping, vomiting, and diarrhea. Pulse and respiration become weak, slow, and irregular. Irritation of the urinary tract and central nervous system resembles alcoholic intoxication.
The airway should be secured and breathing assessed. Other therapies are supportive (intravenous fluids, oxygen, etc.).
poisoning by unknown substances
CAUTION!Many drugs interact with warfarin. To prevent problems with clotting or bleeding, patients taking anticoagulants should consult with health care professionals before adding or deleting medicines from their drug regimens.
The patient is instructed to observe for signs of bleeding such as epistaxis, bleeding gums, hematuria, hematochezia, hemetemesis, melena, and bleeding into the skin (ecchymosis, purpura, or petechia). The importance of regular blood tests (to assess the prothrombin time and international normalized ratio) and medical follow-up is stressed. Maintaining constant intake levels of foods containing vitamin K also is stressed, as intermittent intake can result in widely varied coagulation levels. The patient should wear or carry a medical identification tag listing the prescribed drug, dosage, and frequency of administration. Patients who have mild to moderately elevated INRs should be treated with vitamin K; patients who have serious bleeding and warfarin poisoning should be treated emergently with infusions of prothrombin complex concentrate, factor IX complex concentrate, and recombinant activated factor VII. If these are not readily available, fresh frozen plasma may be used.